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Merck
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安全性情報

SML1923

Sigma-Aldrich

A-395 hydrochloride

≥98% (HPLC)

別名:

(3R,4S)-1-(7-Fluoro-2,3-dihydro-1H-inden-1-yl)-4-{4-[4-(methanesulfonyl)piperazin-1-yl]phenyl}-N,N-dimethylpyrrolidin-3-amine hydrochloride

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About This Item

実験式（ヒル表記法）:
C26H35FN4O2S · xHCl
CAS番号:
2089148-72-9
分子量:
486.65 (free base basis)
MDL番号:
MFCD31563589
UNSPSCコード:
12352200
NACRES:
NA.77

品質水準

100

アッセイ

≥98% (HPLC)

形状

powder

保管条件

desiccated

色

white to light brown

溶解性

H2O: 10 mg/mL, clear

保管温度

2-8°C

SMILES記法

FC1=CC=CC2=C1C(N3C[C@H](C(C=C4)=CC=C4N5CCN(S(C)(=O)=O)CC5)[C@@H](N(C)C)C3)CC2

生物化学的／生理学的作用

A-395 is a potent and selective chemical probe for the polycomb protein EED (embryonic ectoderm development), an essential component of Polycomb repressive complex 2 (PRC2), involved in transcriptional repression through methylation of histone H3K27. A-395 has been found to bind to EED in vitro with a Ki value of 0.4 nM, inhibit the PRC2 complex with an IC50 value 34 nM for methylation of H3K27, and have >100-fold selectivity over other histone methyltransferases and non-epigenetic targets. In RD rhabdoid tumor cell line A-395 inhibited the PRC2 complex with an IC50 value of 90 nM, inhibiting the formation of H3K27me3. For characterization details of A-395, please visit the A-395 probe summary on the Structural Genomics Consortium (SGC) website.

A-395N is the negative control for the active enantiomer, A-395. A-395N is available from Sigma. To learn more about and purchase A-395N, click here.

To learn about other SGC chemical probes for epigenetic targets, visit sigma.com/sgc

特徴および利点

A-395 is an epigenetic chemical probe available through a partnership with the Structural Genomics Consortium (SGC). To learn more and view other SGC epigenetic probes, visit sigma.com/SGC.

ピクトグラム

Skull and crossbones
GHS06

シグナルワード

Danger

危険有害性情報

H301,H315,H319

危険有害性の分類

Acute Tox. 3 Oral - Eye Irrit. 2 - Skin Irrit. 2

保管分類コード

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

引火点(°F)

Not applicable

引火点(℃)

Not applicable

適用法令

試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。

Jan Code

SML1923-VAR:
SML1923-25MG:
SML1923-5MG:
SML1923-BULK:
SML1923-BULK-CR:

試験成績書（COA）

製品のロット番号・バッチ番号を入力して、試験成績書（COA） を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。

以前この製品を購入いただいたことがある場合

文書ライブラリで、最近購入した製品の文書を検索できます。

文書ライブラリにアクセスする

Coral K Wille et al.
Science advances, 9(46), eadf3980-eadf3980 (2023-11-17)
Embryonic stem cells (ESCs) have transcriptionally permissive chromatin enriched for gene activation-associated histone modifications. A striking exception is DOT1L-mediated H3K79 dimethylation (H3K79me2) that is considered a positive regulator of transcription. We find that ESCs are depleted for H3K79me2 at shared
Hywel Dunn-Davies et al.
Molecular therapy. Nucleic acids, 35(2), 102173-102173 (2024-04-15)
Epigenetic processes involving long non-coding RNAs regulate endothelial gene expression. However, the underlying regulatory mechanisms causing endothelial dysfunction remain to be elucidated. Enhancer of zeste homolog 2 (EZH2) is an important rheostat of histone H3K27 trimethylation (H3K27me3) that represses endothelial
Jie Yang et al.
eLife, 12 (2023-09-12)
Human health is facing a host of new threats linked to unbalanced diets, including high-sugar diet (HSD), which contributes to the development of both metabolic and behavioral disorders. Studies have shown that diet-induced metabolic dysfunctions can be transmitted to multiple
Anne-Marie W Turner et al.
ACS infectious diseases, 6(7), 1719-1733 (2020-04-30)
A hallmark of human immunodeficiency type-1 (HIV) infection is the integration of the viral genome into host chromatin, resulting in a latent reservoir that persists despite antiviral therapy or immune response. Thus, key priorities toward eradication of HIV infection are
Alastair Davies et al.
Nature cell biology, 23(9), 1023-1034 (2021-09-08)
Cancers adapt to increasingly potent targeted therapies by reprogramming their phenotype. Here we investigated such a phenomenon in prostate cancer, in which tumours can escape epithelial lineage confinement and transition to a high-plasticity state as an adaptive response to potent

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